Protective effect of resveratrol on acrylamide-induced renal impairment

Nasralla, Mogeda M.; Zaki, Sherif Mohamed; Attia, Rasha Abdel-Monem Hassan

doi:10.5603/fm.a2020.0133

Cited by 5 publications

(4 citation statements)

References 25 publications

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“…The kidney is a critical organ in maintaining electrolyte homeostasis and acid–base balance as well as excreting metabolic wastes . Abnormal renal indicators and histopathological damage caused by AA intake have been previously demonstrated. , Correspondingly, we found that exposure to AA caused renal insufficiency together with a significantly higher level of BUN and Cr, which were decreased after allicin treatment. The transmembrane glycoprotein KIM-1 is known as a hallmark of renal tubular injury, and it is notably elevated in the early phase of kidney injury .…”

Section: Discussionsupporting

confidence: 71%

“…In vivo , highly water-soluble AA can enter organs and tissues, leading to genotoxicity, neurotoxicity, and reproductive toxicity . In the kidney tissues, AA exposure can induce nephrotoxicity, including glomerular edema and congestion, tubular vacuolization, tubular necrosis, and inflammatory cell infiltration …”

Section: Introductionmentioning

confidence: 99%

“…3 In the kidney tissues, AA exposure can induce nephrotoxicity, including glomerular edema and congestion, tubular vacuolization, tubular necrosis, and inflammatory cell infiltration. 4 The kidney is rich in mitochondria, second only to the heart. 5 Mitochondria not only provide energy to the kidney but sense and react to kidney injury through regulating interconnected processes, including mitochondrial dynamics (fission and fusion) and mitophagy, which are essential for maintaining physiological functions.…”

Section: ■ Introductionmentioning

confidence: 99%

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Allicin Alleviates Mitochondrial Dysfunction in Acrylamide-Induced Rat Kidney Involving the Regulation of SIRT1

Li,

Wang,

et al. 2023

J. Agric. Food Chem.

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Acrylamide (AA), commonly formed in carbohydrate-rich thermally processed foods, exerts harmful effects on the kidney. Allicin, from crushed garlic cloves, exhibits strong biological activities. In the current study, the protection mechanisms of allicin against AA-caused nephrotoxicity were comprehensively examined using an in vivo rat model based on previous research that allicin plays a key role in improving renal function. The results showed that allicin attenuated histological changes of the kidney and ameliorated renal function. Damaged mitochondrial structures, upregulated voltage-dependent anion channel 1 expression, and decreased membrane potential and adenosine 5′-triphosphate levels were observed after AA treatment. Surprisingly, allicin notably reversed the adverse effects. Further, allicin effectively restored mitochondrial function via modulating mitochondrial biogenesis and dynamics, which might be associated with the upregulated expression of sirtuin 1 (SIRT1). Meanwhile, allicin dramatically activated the SIRT1 activity and subsequently inhibited p53 acetylation, prevented the translocation of cytochrome c to the cytoplasm, and reduced the caspase expression, thus further inhibiting mitochondrial apoptosis caused by AA. In summary, the relieving effect of allicin on AA-caused nephrotoxicity lies in its inhibition of mitochondrial dysfunction and mitochondrial apoptosis.

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Section: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Section: ■ Introductionmentioning

confidence: 99%

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Allicin Alleviates Mitochondrial Dysfunction in Acrylamide-Induced Rat Kidney Involving the Regulation of SIRT1

Li,

Wang,

et al. 2023

J. Agric. Food Chem.

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“…Accumulating findings from animal studies highlighted the detrimental impact of ACR exposure on various tissues, including the liver, nervous system, reproductive organs, and kidneys ( Rajeh and Al-Dhaheri, 2017 ; Mahfouz et al, 2023 ; Mostafa-Hedeab et al, 2023 ). The study conducted by Nasralla et al (2021) revealed that ACR-induced oxidative stress in hepatic and renal tissues was accompanied by activated apoptosis. Another investigation focusing on the renal effects of ACR exposure unveiled significant microarchitectural alterations, such as glomerular renal abnormalities characterized by shrinkage, distortion of glomeruli, wrinkling of basement membranes, and widening of urinary spaces ( Dasari et al, 2018 ; Moawad et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Acrylamide-targeting renal miR−21a−5p/Fibrotic and miR122-5p/ inflammatory signaling pathways and the role of a green approach for nano-zinc detected via in silico and in vivo approaches

Alqahtani,

Alosaimi,

Abdel-Rahman Mohamed

et al. 2024

Front. Pharmacol.

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Introduction: Any disruption in renal function can have cascading effects on overall health. Understanding how a heat-born toxicant like acrylamide (ACR) affects kidney tissue is vital for realizing its broader implications for systemic health.Methods: This study investigated the ACR-induced renal damage mechanisms, particularly focusing on the regulating role of miR-21a-5p/fibrotic and miR-122-5p/inflammatory signaling pathways via targeting Timp-3 and TP53 proteins in an In silico preliminary study. Besides, renal function assessment, oxidative status, protein profile, and the expression of renal biomarkers (Timp-1, Keap-1, Kim-1, P53, TNF-α, Bax, and Caspase3) were assessed in a 60-day experiment. The examination was additionally extended to explore the potential protective effects of green-synthesized zinc oxide nanoparticles (ZNO-MONPs). A four-group experiment including control, ZNO-MONPs (10 mg/kg b.wt.), ACR (20 mg/kg b.wt.), and ZNO-MONPs + ACR was established encompassing biochemical, histological, and molecular levels. The study further investigated the protein-binding ability of ZNO and MONPs to inactivate caspase-3, Keap-1, Kim-1, and TNFRS-1A.Results: ZNO-MONPs significantly reduced ACR-induced renal tissue damage as evidenced by increased serum creatinine, uric acid, albumin, and oxidative stress markers. ACR-induced oxidative stress, apoptosis, and inflammationare revealed by biochemical tests, gene expression, and the presence of apoptotic nuclei microscopically. Also, molecular docking revealed binding affinity between ACR-BCL-2 and glutathione-synthetase, elucidating the potential mechanisms through which ACR induces renal damage. Notably, ZNO-MONPs revealed a protective potential against ACR-induced damage. Zn levels in the renal tissues of ACR-exposed rats were significantly restored in those treated with ACR + ZNO-MONPs. In conclusion, this study establishes the efficacy of ZNO-MONPs in mitigating ACR-induced disturbances in renal tissue functions, oxidative stress, inflammation, and apoptosis. The findings shed light on the potential renoprotective activity of green-synthesized nanomaterials, offering insights into novel therapeutic approaches for countering ACR-induced renal damage.

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The potential role of Tirzepatide as adjuvant therapy in countering colistin-induced nephro and neurotoxicity in rats via modulation of PI3K/p-Akt/GSK3-β/NF-kB p65 hub, shielding against oxidative and endoplasmic reticulum stress, and activation of p-CREB/BDNF/TrkB cascade

Hassan,

Ragab,

Ibrahim

et al. 2024

International Immunopharmacology

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Protective effect of resveratrol on acrylamide-induced renal impairment

Cited by 5 publications

References 25 publications

Allicin Alleviates Mitochondrial Dysfunction in Acrylamide-Induced Rat Kidney Involving the Regulation of SIRT1

Allicin Alleviates Mitochondrial Dysfunction in Acrylamide-Induced Rat Kidney Involving the Regulation of SIRT1

Acrylamide-targeting renal miR−21a−5p/Fibrotic and miR122-5p/ inflammatory signaling pathways and the role of a green approach for nano-zinc detected via in silico and in vivo approaches

The potential role of Tirzepatide as adjuvant therapy in countering colistin-induced nephro and neurotoxicity in rats via modulation of PI3K/p-Akt/GSK3-β/NF-kB p65 hub, shielding against oxidative and endoplasmic reticulum stress, and activation of p-CREB/BDNF/TrkB cascade

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